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Benign Melanocytic Lesions
Published in Ashfaq A Marghoob, Ralph Braun, Natalia Jaimes, Atlas of Dermoscopy, 2023
Valeria De Bedout, Natalia Jaimes
Epidermolysis bullosa (EB) refers to a group of mechanobullous diseases arising from various mutations in keratin proteins at the dermo-epidermal junction. Patients with EB develop blisters and erosions after minor trauma to the skin and mucosae. Depending on the level at which the cleavage occurs, EB has been classified into epidermolytic or simplex, junctional, and dermolytic or dystrophic (20).
Diagnosing Skin Disease
Published in Ayşe Serap Karadağ, Lawrence Charles Parish, Jordan V. Wang, Roxburgh's Common Skin Diseases, 2022
A variety of causes are associated with blistering dermatosis, including autoimmune, infectious, and inflammatory etiologies. Autoantibodies against desmogleins 1 and 3, which are components of desmosomes that keep keratinocytes attached to one another, resulting in acantholysis, or a loss in intercellular connections, and can lead to intraepidermal blisters. In contrast, autoantibodies against components of hemidesmosomes of the dermo-epidermal junction in bullous pemphigoid result in subepidermal blisters (Figure 2.6). Herpesvirus infection of the epidermis may result in acantholysis and varying degrees of epidermal necrosis, which can lead to intraepidermal or subepidermal blisters. Significant intercellular edema in allergic contact or nummular dermatitis results in intraepidermal blisters. Any process that weakens the dermo-epidermal junction may result in a subepidermal blister (Figure 2.7). Severe dermal edema from a variety of sources may also result in a subepidermal blister (e.g., lymphedema blister, bullous insect bite, and bullous Sweet syndrome). Depending on the severity and acuity, most interface dermatitides, which are associated with a variable degree of necrosis of keratinocytes at the dermo-epidermal junction, have a subepidermal bullous expression. Examples include bullous erythema multiforme, bullous lichen planus, and bullous fixed-drug eruption.
An introduction to skin and skin disease
Published in Rashmi Sarkar, Anupam Das, Sumit Sethi, Concise Dermatology, 2021
The junctional zone has considerable functional importance and is vital to understanding the pathophysiology of bullous disorders and many other skin diseases. Figure 1.3 shows the main components of the junctional zone. Desmosomal processes from the basal keratinocytes, known as hemidesmosomes, are inserted into an electron-dense lamina (basal lamina). Below the electron-dense lamina, there is an electron-lucent area (lamina lucida). The dermoepidermal junction is important from the clinical point of view. When the component molecules do not function properly, the adhesive property of the junction is lost and this leads to numerous bullous diseases, including bullous pemphigoid, cicatricial pemphigoid, linear IgA disease, pemphigoid gestationis, epidermolysis bullosa acquisita, etc.
Efficacy and safety of picosecond laser for wrinkle in Indonesian skin
Published in Journal of Cosmetic and Laser Therapy, 2022
Putri Hendria Wardhani, Cita Rosita Sigit Prakoeswa, M. Yulianto Listiawan
This study also demonstrates that the picosecond 755 nm laser with DLA is a safe way to treat wrinkle in darker skin type. The majority of patients had resolution of redness and edema less than 24 hours after treatment. There were no prolonged hyperpigmentation, hypopigmentation, any other dyspigmentations or scarring. A 755 nm picosecond Alexandrite laser with a DLA optic delivered an array of unique, focal zones of intra-epidermal injury in the stratum spinosum characterized by vacuoles at the site of the high fluence zones. As measured with confocal microscopy and H&E staining, the stratum corneum and all tissue surrounding the vacuoles appeared normal with no indication of collateral thermal damage. This injury profile is in stark contrast to epidermal and dermal damage apparent in non-ablative and ablative fractional treatments (9). It has been hypothesized that once LIOB is formed, it absorbs most of the subsequent incoming laser irradiation. These LIOBs are confined to the intraepidermis and have been demonstrated on histology. Normally 755 nm irradiation propagates into the dermoepidermal junction and dermis. However, when LIOB is present it causes a very localized and superficial absorption of the laser irradiation. Therefore, excessive radiation does not reach the dermoepidermal junction, protecting pigment, and minimizing collateral damage. All surrounding tissue structures appear to be undamaged and a significant neocollagenesis and neoelastinogenesis response is stimulated (6,8).
Effect of ultraviolet radiation on the Nrf2 signaling pathway in skin cells
Published in International Journal of Radiation Biology, 2021
Alena Ryšavá, Jitka Vostálová, Alena Rajnochová Svobodová
Due to having the highest energy, UVC radiation has the greatest potential to damage cells, even after short exposure times. It is highly mutagenic as the absorption maximum of DNA is within the UVC waveband (260–265 nm). Fortunately, UVC photons are completely absorbed in the stratospheric ozone layer, together with most UVB photons (100–295 nm) (Svobodová and Vostálová 2010; Ikehata and Yamamoto 2018; Azami et al. 2019). Nevertheless, 5–10% of the UV radiation that reaches the Earth’s surface is UVB. Due to ozone layer depletion, the number of UVB photons reaching the surface of the planet is increasing (Young 2006). UVB is mostly absorbed by the epidermis, the majority (∼70%) in the stratum corneum, which is formed from corneocytes (Kulms et al. 2002; Svobodová and Vostálová 2010). UVA represents up to 95% of the UV rays that reach the Earth’s surface, with no considerable absorption occurring in the ozone layer. UVA radiation is divided into two parts: wavebands UVA1 (400–340 nm) and UVA2 (340–320 nm). Around 80% of UVA reaches the dermo-epidermal junction and penetrates deeper into the papillary dermis. About 10% of UVA even manages to reach the hypodermis (York and Jacobe 2010; Pittayapruek et al. 2016). The amount of solar UV radiation reaching the Earth’s surface, and the UVA/UVB ratio, depend on a number of factors, such as latitude, altitude, season, cloud cover, time of day, and time of year (Young 2006).
A novel treatment for CI extrusion with vacuum-assisted closure device
Published in Cochlear Implants International, 2021
Celeste Ann Chua, Jiun Fong Thong, Siti Radhziah Binte Sudirman
Our patient had presented with a soft tissue infection with flap breakdown 18 years after her cochlear implantation. In a study by Ungar et al. (2018) in 2018 where 236 temporo-parietal scalps were measured in patients aged 18–85 years, scalp thickness decreased with age from a mean of 8 mm in the third decade to 5 mm in the ninth decade. As the skin ages, the subcutaneous layer atrophies as skin appendages become more scarce, blood flow decreases and there is degeneration of the extracellular matrix accompanied by fewer fibroblasts and altered collagen (Makrantonaki and Zouboulis, 2007). In addition, flattening of the dermo-epidermal junction (Burns et al., 2008) and halving of epidermal cell turnover between the third and seventh decades of life (Grove and Kligman, 1983) lead to decreased wound healing capacity (Goodson and Hunt, 1979). It is likely that the thinning of scalp thickness with age contributed to an increased risk of flap breakdown in our patient.